scholarly journals Contribution of Respiratory Muscle Oxygen Consumption to Breathing Limitation and Cyspnea

1997 ◽  
Vol 4 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Pere Casan ◽  
Carlos C Villafranca ◽  
Clive Kearon ◽  
Edward JM Campbell ◽  
Kieran J Killian

During exercise, the sustainable activity of large muscle groups is limited by oxygen delivery. The purpose of this study was to see whether the oxygen consumption of the respiratory muscles reaches a similar critical value under maximal resistive loading and hyperventilation. A secondary objective was to see whether dyspnea (estimated discomfort experienced with breathing using the Borg 0-10 scale) and the oxygen consumption of the respiratory muscles are closely related across conditions. This would be expected if intramuscular sensory nerve fibres stimulated as a consequence of metabolic events contributed to this sensation. In six normal subjects the respiratory muscles were progressively activated by the addition of incremental inspiratory resistive loads to a maximum of 300 cm H20×s/L (SD=66.4), and incremental dead space to a maximum of 2638 mL (SD=452), associated with an increase in ventilation to 75.1 L/min (SD=29.79). Each increment was maintained for 5 mins to allow the measurement of oxygen uptake in a steady state. During resistive loading total oxygen consumption increased from 239 mL/min (SD=38.2) to 299 mL/min (SD=52.3) and dyspnea increased to "very severe" (Borg scale 7.5, SD=1.55). During dead space loading total oxygen consumption increased from 270 mL/min (SD=20.2) to 426 mL/min (SD=81.9) and dyspnea increased to "very severe" (7.1, SD=0.66). Oxygen cost of inspiratory muscle power was 25 mL/watt (95% confidence limits 16.7 to 34.3) with dead space loading and 91 mL/watt (95% confidence limits 54 to 128) with resistive loading. Oxygen consumption did not reach a critical common value in the two types of loading, 60 mL/min (SD 22.3) during maximal resistive loading and 156 mL/min (SD 82.4) during maximal dead space loading (P<0.05). Physiological factors limiting the respiratory muscles are not uniquely related to oxygen consumption and appear to be expressed through the activation of sensory structures, perceptually manifested as dyspnea.

1960 ◽  
Vol 15 (3) ◽  
pp. 359-362 ◽  
Author(s):  
G. Milic-Emili ◽  
J. M. Petit

Simultaneous measurements of mechanical work and energy cost of breathing were performed on four normal subjects with ventilation increased by adding dead space. Mechanical work was obtained from simultaneous records of endoesophageal pressure and tidal volume. The associated energy cost was estimated by measuring oxygen consumption of respiratory muscles by means of a closed-circuit spirometer. In all subjects studied and over the range of ventilations involved (ca. 30–110 l/min.), the mechanical efficiency of breathing was found to be in the order of 0.19–0.25. Submitted on July 6, 1959


2019 ◽  
Vol 6 (3) ◽  
pp. 64-67
Author(s):  
Omer Abdalla Elbedri Abdalla ◽  
Omer A Musa

Airway function is one of the many biologic functions that exhibit circadian variability over 24-h periods. Studies of circadian variability of lung function in normal subjects as well as asthmatics are particularly scarce, and those of MEP and MIP are unknown. The aim of this study to determine circadian variation in lung function (FVC, FEV1 and PEFR) and respiratory muscle pressures(MEP and MIP) for measurement of respiratory muscle power at 6:00am (early morning),12:00midday, 6:00pm( evening) and 12:00 midnight in healthy subjects and in patients with mild asthma at 6:00am and 6:00pm , to elaborate on the possibility of using MEP and MIP variability as a new diagnostic test for asthma. This is a cross sectional study performed in Khartoum, the capital of Sudan during December 2010. Thirty healthy, symptoms free non smokers normal subjects aged 20-64 years selected randomly and 15 mild asthmatics, clinically free during the time of study aged 19-49 years were included in the study. There is significant drop in healthy subjects early in the morning compared to 6:00pm, the drop in FVC was 9.75%, in FEV1 was 8.79%, in PEFR was 8.44%, in MEP was 10.04%, and in MIP was 17.57%. There is also significant drop in asthmatics early in the morning in MEP and MIP (21.76%, 27.57% respectively), is comparable to FEV1 (22.56%) and PEFR (23.86%). The sensitivity and specificity of variability for MEP (53%, 77%) and MIP (60%, 63%) comparable to sensitivity and specificity of FEV1 variability (40%, 86%) and PEFR variability (46%, 73%). The obtained comparable results of MEP, MIP variability to FEV1, PEFR variability in normal and asthmatic subjects could imply that MEP & MIP can be used in assessing airway calibre as in asthma. The study concluded that MEP & MIP variability could be sensitive tests to confirm asthma diagnosis.


1987 ◽  
Vol 73 (6) ◽  
pp. 627-634 ◽  
Author(s):  
R. Lane ◽  
L. Adams ◽  
A. Guz

1. The effect of adding low-level (2.7 cmH2O 1−1 s) external respiratory resistive loads on exercise-induced breathlessness has been examined in naive normal subjects; the intensity of this loading was chosen to simulate that confronting an asthmatic subject during exercise. 2. Each of 18 subjects performed two separate tests in which workload was oscillated while the respiratory loading was changed every minute between no loading, inspiratory loading only, and inspiratory plus expiratory loading. Each loading condition was given three times, and both these changes and those in workload were unpredictable as far as the subject was concerned. 3. The purpose was to ‘confuse’ subjects and obtain subjective estimates of their intensity of breathlessness independent of any expectation associated solely with the readily perceptible changes in external resistances to breathing. The study design was balanced for the group as a whole, both in terms of workload and respiratory loading condition. 4. The addition of these respiratory resistive loads during exercise did not result in a significant increase in the intensity of breathlessness. 5. Estimates of the rate of work of breathing revealed that this increased more with respiratory loading than it did as ventilation rose throughout the test; on the other hand, the intensity of breathlessness increased by a greater extent with continued exercise compared with the changes accompanying the addition of respiratory loads. 6. It is concluded that the intensity of the sensation of breathlessness experienced by normal subjects during exercise is not simply a reflection of an increased rate of work of breathing being performed by the respiratory muscles. 7. It is further suggested that similar studies in which internal resistances are increased experimentally are indicated in order to analyse the factors underlying the breathlessness of asthma.


2010 ◽  
Vol 25 (1) ◽  
pp. 45-48
Author(s):  
Kenichi ORIMOTO ◽  
Ayako UEJYO ◽  
Hideaki SENJYU

1990 ◽  
Vol 69 (1) ◽  
pp. 14-20 ◽  
Author(s):  
T. Takishima ◽  
C. Shindoh ◽  
Y. Kikuchi ◽  
W. Hida ◽  
H. Inoue

The first purpose of the present study was to develop a new method to examine oxygen consumption of respiratory muscles (VO2resp) in human subjects. The apparatus consists of an expandable dead space and a respirometer. When the dead space was increased at a constant rate (approximately 100 ml/min), minute ventilation (VE) and VO2resp increased gradually. Because the logarithm of VO2 was found to be approximately linearly related to VE, we characterized this relationship by the slope (logVO2/VE) and the intercept at VE = 0 (VO2met) of the semilog regression line. The second purpose of this study was to examine the relationship between VO2resp and aging. Six anthropometric and spirometric factors (age, height, weight, vital capacity, forced expiratory volume in 1 s, and body surface area) were analyzed in 37 normal subjects by simple and stepwise multiple regression analyses. We found a significant increase in logVO2/VE and a significant decrease in VO2met with age. In conclusion, 1) the present method is convenient to use, and we are able to study VO2resp over a wide range of ventilation without voluntary effort, and 2) age per se is one of the factors accounting for the observed increase in VO2resp with age.


1967 ◽  
Vol 28 (6) ◽  
pp. 1042-1047 ◽  
Author(s):  
Richard A. Theye

1984 ◽  
Vol 246 (3) ◽  
pp. R380-R383 ◽  
Author(s):  
C. Martinez-Torres ◽  
L. Cubeddu ◽  
E. Dillmann ◽  
G. L. Brengelmann ◽  
I. Leets ◽  
...  

Twenty-one Venezuelan peasants were segregated into three groups on the basis of measurements of iron status: seven normal subjects, six iron-deficient subjects with normal hemoglobin and eight iron-deficient subjects with a hemoglobin concentration of less than 9 g/dl. All subjects were placed in a water bath at an initial temperature of 36 degrees C. The water temperature was then rapidly lowered to 28 degrees C, and observations were made over the period of 1 h. Mean oral temperature of the first group fell 0.2, the second group 0.5, and the third group 0.9 degrees C. Mean plasma norepinephrine levels in both groups of iron-deficient subjects were significantly higher at 36 degrees C and during cold exposure compared with control subjects. Oxygen consumption was also significantly increased in both groups of iron-deficient subjects after cold exposure.


1987 ◽  
Vol 131 (1) ◽  
pp. 137-157
Author(s):  
D. F. HOULIHAN ◽  
C. AGNISOLA ◽  
N. M. HAMILTON ◽  
I. TRARA GENOINO

A technique is described which allowed the measurement of the oxygen consumption of the isolated heart of Octopus vulgaris. Contraction of the heart resulted in an aortic output and a flow through the heart muscle into coronary veins (the coronary output). The flow and oxygen content of the aortic output and the coronary output were measured with variable input pressures and constant output back pressure (volume loaded), variable output back pressure and constant aortic output (pressure loaded), and during hypoxia. Volume loading of the heart resulted in an increase in aortic output, power output and total oxygen consumption. Pressure loading increased power output and total oxygen consumption of the heart. Exposure to hypoxia decreased the aortic output, power output and total cardiac oxygen consumption. In the response of the heart to reduced work, brought about either by a reduced input pressure or by hypoxic perfusate, the power output was linearly related to the total oxygen consumption of the heart. The oxygen extracted from the coronary output accounted for 80–100% of the total oxygen consumption of the heart. Coronary output amounted to 30% of the total cardiac output at maximum power output. In volume-loaded hearts the volume of the coronary output increased as aortic output increased; in pressure-loaded hearts coronary output increased as power output increased, but aortic output remained constant. In hypoxia, the coronary output increased as the aortic output fell. At a perfusate Po2 of around 50 Torr (1 Torr = 133 Pa), the aortic output ceased although the heart continued to beat and the coronary output continued, accounting for all of the oxygen consumption of the heart. The coronary output flow in vitro therefore has the capacity to be varied independently of the aortic output flow to maintain the oxygen supply to the perfused cardiac muscle.


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